TERC telomerase subunit gene copy number in placentas from pregnancies complicated with intrauterine growth restriction

被引:33
作者
Biron-Shental, Tal [1 ,2 ]
Kidron, Dvora [2 ,3 ]
Sukenik-Halevy, Rivka [1 ,4 ]
Goldberg-Bittman, Lilach [4 ,5 ]
Sharony, Reuven [1 ,2 ,3 ]
Fejgin, Moshe D. [1 ,2 ,3 ,4 ]
Amiel, Aliza [4 ,5 ]
机构
[1] Meir Med Ctr, Dept OBGYN, IL-44821 Kefar Sava, Israel
[2] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel
[3] Meir Med Ctr, Dept Pathol, IL-44821 Kefar Sava, Israel
[4] Meir Med Ctr, Genet Inst, IL-44821 Kefar Sava, Israel
[5] Bar Ilan Univ, Fac Life Sci, Ramat Gan, Israel
关键词
TERC; IUGR; FISH; Trophoblasts; Placenta; HUMAN FIBROBLASTS; CELL-CULTURES; RNA COMPONENT; LIFE-SPAN; FETAL; HYBRIDIZATION; SENESCENCE; CANCER;
D O I
10.1016/j.earlhumdev.2010.08.024
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Introduction: Intrauterine growth restriction (IUGR) is a significant cause of both short-and long-term morbidity and mortality. IUGR secondary to placental dysfunction is correlated with telomere shortening. Telomerase is an enzyme complex that elongates telomeres. One of its components is encoded by the telomerase RNA component gene (TERC), which serves as the RNA template for the addition of telomeric repeats. We hypothesized decreased TERC gene copy number in IUGR placentas as part of the mechanism of telomere shortening in placental dysfunction. Methods: We estimated the gene copy number of the TERC gene at 3q26 by applying FISH to trophoblasts of placental biopsies from five pregnancies with IUGR caused by placental insufficiency and compared them to placentas from five gestational-age matched, uncomplicated pregnancies. Results: Significantly lower TERC gene copy number was observed in IUGR trophoblasts on the same chromosome and on other chromosomes, compared to the control samples (p<0.05). Conclusions: The TERC gene copy number is decreased in IUGR trophoblasts. These results support the observations of telomere shortening and decreased telomerase activity in IUGR placentas. We suggest that these findings might play a role in the pathophysiology of IUGR, perhaps by promoting senescence in trophoblasts of IUGR placentas. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:73 / 75
页数:3
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